title: Healing human myocardial infarction associated with increased chymase immunoreactivity.
abstract: We studied the immunoreactivity of the chymase protein in normal human myocardium and in human myocardial infarctions at various postinfarction times using immuno-histochemistry. In noninfarcted hearts chymase was mainly present in cardiomyocytes and endothelial cells. At 6 h after infarction the ischemic cardiomyocytes had lost their chymase immunoreactivity. A portion of the smooth muscle alpha-actin-expressing myofibroblasts and some of the CD-68-positive macrophages, which both appear 4-6 days after infarction, contained chymase. Chymase was also found in mast cells, which were present in the normal myocardium and the healing scar. These data show that chymase, a protein that mediates the conversion of angiotensin I to angiotensin II via a non-angiotensin-converting-enzyme-dependent pathway is present in the normal adult human myocardium and is upregulated in the healing tissue after myocardial infarction.
authors.affiliation: Department of Pathology, Cardiovascular Research Institute Maastricht, University of Maastricht, The Netherlands.
authors.forename: M J
authors.initials: MJ
authors.lastname: Daemen
authors.forename: H
authors.initials: H
authors.lastname: Urata
mesh_terms: D053818:Chymases; D006801:Humans; D007124:Immunoenzyme Techniques; D009203:Myocardial Infarction / Q000201:enzymology* / Q000473:pathology; D009206:Myocardium / Q000166:cytology / Q000201:enzymology*; D012697:Serine Endopeptidases / Q000378:metabolism*
chemical_list: D012697:Serine Endopeptidases; D053818:Chymases